Atopic dermatitis (AD) is an inflammatory skin disease, in which epidermal barrier impairment, often owing to FLG null mutations, precedes immune hyper-responsiveness. Ichthyosis vulgaris (IV) is characterized by FLG null mutations and non-inflammatory dry skin. SPINK5 null mutations in Netherton syndrome (NS) lead to erythroderma and atopic manifestations. Thus, AD, IV and NS share clinical, genetic or immunological similarities. We sought to evaluate effects of specific skin disease features i.e. ichthyotic and/or atopic manifestations on bacterial and fungal microbiota. The bacterial and fungal skin microbiota was determined by using 16S rRNA (V4) and ITS gene sequencing and the Illumina MiSeq platform at two body sites in  patients with AD with or without FLG null mutations or skin lesions, IV or NS and in healthy donors. We found that bacterial richness and evenness were suggested to greater variations than those of fungi in response to skin diseases. Severity of epidermal barrier impairment controlled bacterial but not fungal skin composition. Proportions of Firmicutes (Staphylococcaceae) and Actinobacteria (Corynebacteriaceae) were augmented in ichthyoses and lesional AD, whereas proportions of Proteobacteria and Bacteroidetes were reduced, regardless of body sites. Ascomycota were increased in AD and NS but owing to the expansion of different fungal species. Potentially pathogenic bacteria (Staphylococci and Corynebacteria) were particularly abundant in IV and NS. Severity of epidermal barrier impairment superseded physicochemical properties of body sites to alter skin bacterial communities but had no effects on fungal microbiota. Thus, distinguishable bacterial and fungal dysbiosis in AD, NS, and IV emphasizes disease-specific pathomechanisms.

Distinguishable bacterial and fungal dysbiosis in skin of patients with Atopic Dermatitis or Netherton Syndrome.